1. Field of the Invention
The present invention relates to the field of phytodrugs, and in particular the invention relates to phytodrugs for management of peptic ulcer conditions in humans and methods of preparing and using same.
2. Prior Activities and Problems in the Field
Peptic ulcer has been defined as a benign lesion of gastric or duodenal mucosa occurring at a site where the mucosal epithelium is exposed to acid and pepsin. It is a gastro-intestinal problem that has been prevalent in society. The occurrence of the disease has been associated with over-indulgence, inappropriate habit, anxiety and stress. Considerable energy and resources have been expended towards relieving symptoms of peptic ulcer which usually manifests as an excruciating pain, especially in the upper abdomen. For centuries neutralization of gastric acid secretion with antacids and H2-receptor antagonists, provide the only relief from the pains of peptic ulcer. The drugs are generally expensive. Consequently, the socioeconomic impact of peptic ulcer disease on the society can only be imagined.
In the foregoing assertion, efforts have been made to find a suitable palliative and/or curative agent for the treatment of peptic ulcer conditions from medicinal plants.
It is estimated that approximately 10% of most populations globally will develop severe peptic ulcer conditions at some time during their lifetime. The lesions occur at all ages and affect both sexes.
Authorities estimate that at least five million people suffer from active peptic ulcers each year, and approximately 350,000 to 500,000 new cases are diagnosed annually in the United States alone. More than 600,000 patients are hospitalized in the U.S. each year for severe episodes. In approximately one-third of these cases serious complications occur, including intestinal obstruction, upper gastrointestinal hemorrhage and perforation. Furthermore, each year, over 6,000 deaths in the U.S. are directly caused by ulcer disorder. In addition, peptic ulcer conditions have been implicated as an indirect contributing factor in an additional 11,000 deaths each year.
In Nigeria, peptic ulcer conditions general afflict persons between the ages of 21 and 51. Duodenal ulcers have their greatest impact in middle age while gastric ulcers become increasingly more frequent with advancing age.
Peptic ulceration reflects an imbalance between the aggressive action of acid peptic secretions and the defensive forces that protect the mucosa. Gastric ulcers result from lowered defensive mechanisms and duodenal ulcers are the consequence of the destructive action of increased acid-peptic secretions.
Duodenal ulcers occur when gastric mucosa secretes substantial amounts of acid. Although some patients with duodenal ulcers have normal levels of acid secretion, on the average they are hyperchlorhydric. Gastric acid has two phases viz;
(1) a cephalic phase (vagally mediated) in which direct cholinergic stimulation of parietal cells induces gastrin release from the antrum, and PA1 (2) a less powerful antral phase when food enters the stomach, causing liberation of more gastrin from the antral mucosa.
Evidence that patients with duodenal ulcers have increased parietal cell mass also suggests a genetic predisposition even though experimental data indicate that parental cell hyperplasia can be acquired.
Gastric ulceration results from lowering of the gastric mucosal resistance. Principal among the defensive influences is mucous secretion. The increased frequency of gastric ulcers with advancing age might be compatible with progressive inability to secrete a protective layer of mucous. Chronic gastritis is a frequent concomitant of gastric ulcer, is associated with impaired mucous secretion and is also age-related. In experimental animals, it has been demonstrated that protein depletion, avitaminoses and general malnutrition increase the susceptibility to gastric ulceration.
There is now growing evidence that Helicobactor pylori, a bacterium may be the cause of duodenal ulcer. The evidence linking Helicobactor pylori with benign gastric ulcer is less convincing than duodenal ulcer. However, the consensus now is that the organism is probably important in the pathogenesis of 70% of gastric ulcers not attributable to the use of non-steroidal anti-inflammatory drugs (NSAIDS).
The symptoms evoked by peptic ulcers are exceedingly variable; some ulcers being virtually asymptomatic. Nausea and vomiting may be produced by either duodenal or gastric ulcers, but particularly by the latter. The most consistent manifestation is epigastric pain described variably as burning, gnawing or boring. Classically, the duodenal ulcer pain becomes most severe two or three hours after the last meal and persists until it is relieved by food or antacids. For this reason, the pain recurs in the middle of the night and requires a glass of milk or antiacid for its relief. Such episodic pain may last for weeks or months only to abate, usually with regulated dietary regimen and therapy. Recurrence is often triggered by dietary indiscretions or stress and is usually very rapid and sometimes dramatic, presenting with hemorrhage or perforation. Death from peptic ulcer is usually due to bleeding or perforation. In addition, a high proportion of patients who die or whose ulcers bleed or perforate have no warning signals.